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作 者:栾少华 王洋 张长柱(综述) 王楠(审校) LUAN Shaohua;WANG Yang;ZHANG Changzhu;WANG Nan(Department of Procurement Management,General Hospital of Eastern Theater Command,PLA,Nanjing 210002,Jiangsu,China;Department of Pharmacy,Anhui Medical University Hospital,Hefei 230032,An-hui,China)
机构地区:[1]东部战区总医院采购管理科,南京210002 [2]安徽医科大学医院药剂科,合肥230032
出 处:《医学研究与战创伤救治》2024年第10期1114-1120,共7页Journal of Medical Research & Combat Trauma Care
摘 要:持续的炎症和肝星状细胞(HSCs)的激活是肝纤维化发生的主要因素,炎症引起细胞释放炎症因子,能增强免疫功能、调节体温、抑制癌细胞增殖等,但持久反复的炎症反应将会引起肝纤维化。在炎症小体家族中,核苷酸结合寡聚化结构域样受体3(NLRP3)炎症小体越来越多的证明了在肝纤维化发病机制中的重要作用,尤其是NLRP3炎症小体可通过诱导HSCs的活化加重肝纤维化。文章主要就NLRP3炎症小体在HSCs活化中的作用机制以及治疗前景进行综述。Persistent inflammation and the activation of hepatic stellate cells(HSCs)are major factors in the development of hepatic fibrosis.Inflammation induces the release of inflammatory factors from cells,which enhances immune function,regulates body temperature,and inhibits the proliferation of cancerous cells,etc.However,persistent and repeated inflammatory responses will cause hepatic fibrosis.Among the family of inflammasomes,NLRP3 inflammasome has increasingly demonstrated an important role in the pathogenesis of hepatic fibrosis,and in particular,NLRP3 inflammasome can exacerbate hepatic fibrosis by inducing the activation of HSCs.Therefore,the mechanism of the role of NLRP3 inflammasome in the activation of HSCs and the therapeutic perspectives are focused in this review.
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